An Itchy Situation

November 2, 2013 by

Nov. 1, 2013

By Medical Discovery News

Anyone ever bitten by a mosquito can attest to its itchy consequences. New research has discovered just how our bodies detect and process itching, leading to a better understanding of our reaction to itching and hopefully better treatments for it.

The clinical term for an itch is pruritus, and at least 16 percent of people experience an itch that just doesn’t go away. The most common dermatological complaint, long-term itching can be caused by chronic renal disease, cirrhosis, some cancers, multiple sclerosis, diabetes, shingles, allergic reactions, drug reactions, and pregnancy.

Prolonged itching and scratching can increase the intensity of the itch, possibly leading to neurodermatitis, a condition in which a frequently scratched area of skin becomes thick and leathery. The patches can be raw, red, or darker than the rest of the skin. Persistent scratching can also lead to a bacterial skin infection, permanent scars, or changes in skin color. The super strong pain reliever morphine can cause such a severe whole-body itch that some patients choose to forgo it and live with the pain.

Sensory neurons called TRPV1 cells detect itchy substances on skin. TRPV1 cells have long nerve fibers that extend into skin, muscle, and other tissues to help monitor conditions. It has not been clear how these neurons sort through different sensations like pain and temperature and route the signal along the proper pathway to the appropriate area of the brain for perception.

New research has revealed a small group of those neurons produce a substance called natriuretic polypeptide b (Nppb), a hormone known to be involved in regulating the heart. Surprisingly, when Nppb is produced by TRPV1 cells it acts as a neurotransmitter, a chemical messenger secreted by neurons to carry, boost, and control signals between neurons and other cells.

When scientists genetically modified mice to eliminate Nppb, they did not itch. Nppb binds to a specific receptor called Npra on particular nerves in the spinal column. When those cells were eliminated in mice, again, they did not itch. Interestingly, removing these cells did not impact other sensory sensations such as temperature, pain, and touch.

A similar transmission presumably exists in humans, but that has not yet been determined. Knowing which molecules and cells are involved will help scientists study how humans perceive itch signals. Before these findings, scientists thought a molecule called gastrin releasing peptide was responsible for transmitting the itch signal from nerves, and that itching was a low level form of pain.

Understanding the itch signaling pathway offers the opportunity to create drugs that specifically block that signal and alleviate unpleasant and chronic itching with fewer side effects.

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Aging But Still Protected

June 14, 2013 by

June 14, 2013

By Medical Discovery News

The people who are at the highest risk of dying from common infections like pneumonia, influenza, and colds are 50 and older. Traditionally, scientists believed that as we age, our immune systems weaken, leaving us more vulnerable than ever to infections. But new research suggests that this isn’t completely true – certain parts of the immune system remain fully functional and robust longer.

It is true that older people make fewer antibodies, proteins that attach to viruses and cells infected with viruses to mark them for elimination by the immune system. This explains why some vaccines aren’t as effective in the elderly. The flu vaccine, for example, contains a “dead” virus that stimulates the body to make more protective antibodies against the flu.

However, other vaccines are well-received in older people, like the varicella zoster virus vaccine that prevents shingles. This vaccine does not involve antibodies, but T-cells, which kill infected cells, and memory T-cells, which recognize and respond to a reinfection.

White blood cells, formally called leukocytes, represent an army ready to defend the body from bacterial or viral attacks. T-cells are one type of soldier in this army, responsible for cellular immunity – killing infected cells to protect the body. The thymus, located between the breast bone and heart, produces T-cells. But as people age, the thymus does too.

The thymus shrinks by about 3 percent a year during middle age, and there is a corresponding fall in the production of T-cells. As humans age, their T-cells increasingly become memory cells. Therefore, it’s been assumed that the T-cell response to kill cells infected with a virus is impaired in older adults, making them more susceptible to viral infections.

To test that assumption, researchers at the McMaster Immunology Research Centre in Ontario isolated blood from people with one of three types of viral infections: West Nile Virus, Epstein-Barr Virus, and Cytomegalovirus. They divided the patients into three groups: those under 40, those middle-aged (41 – 59), and those over 60. They then measured the amount, type, and activity of the T-cells in each group. The older group did indeed have a shift toward the production of memory T-cells. But surprisingly, the amount of virus-specific T-cells did not decrease with age – the older group had roughly the same amount as the middle and younger groups.

These results suggest that the thymus continues to play an important role in producing T-cells that target viral infections as we age. It also indicates that vaccines designed to stimulate cellular immunity, instead of antibodies, would be more effective in older people. So the flu vaccine might prevent more flu cases in older people if the dead virus was replaced with a live but weakened virus, but currently that’s not approved in the U.S. for people over 50.

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